A 3rd shot? A new booster? Vaccine makers race to trials to beat variants

COVID-19 vaccine at a vaccination center in Madrid on Feb. 26, 2021.

Enlarge / COVID-19 vaccine at a vaccination center in Madrid on Feb. 26, 2021. (credit: Getty | NurPhoto)

With worrisome coronavirus variants seemingly emerging and spreading everywhere, lead vaccine makers are wasting no time in trying to get ahead of the growing threat.

This week, Moderna and partners Pfizer and BioNTech announced they have kicked off new vaccine clinical trials aimed at boosting the effectiveness of their authorized vaccines against new, concerning SARS-CoV-2 variants—primarily B.1.351, a variant first identified in South Africa.

In a set of studies published last week in the New England Journal of Medicine, both the Moderna mRNA vaccine and Pfizer/BioNTech mRNA vaccine spurred antibodies in vaccinated people that could neutralize the B.1.351 variant. But the levels of those neutralizing antibodies were significantly lower than what was seen against past versions of the virus. (Both vaccines performed well against the B.1.1.7 variant, first identified in the UK, which is expected to become the dominant strain in the US next month.)

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B.1.1.7 coronavirus variant is picking up a worrisome new mutation

Cartoon representation of coronaviruses.

Enlarge (credit: CDC.gov)

As the world races to get vaccines into arms, one of the most concerning coronavirus variants appears to be getting a little more concerning.

Researchers in the UK have detected at least 15 cases of B.1.1.7 variants carrying an additional mutation: E484K, a mutation already seen in other concerning variants and one that may make current vaccines less effective at preventing infection. The B.1.1.7 variant, first identified in the United Kingdom, is already known to spread more easily among people than earlier strains of the pandemic coronavirus SARS-CoV-2. And according to some preliminary evidence, it may cause more severe disease.

So far, B.1.1.7 variants carrying E484K appear rare. On Monday, Public Health England reported in a technical briefing that it had detected E484K in just 11 B.1.1.7 variants among more than 200,000 viruses examined. For now, it’s unclear if the augmented mutants will take off and become dominant in the population or fizzle out. It’s also not entirely clear what the addition of E484K means for B.1.1.7 in people. Preliminary laboratory experiments suggest the mutation alone, and its presence in B.1.1.7 specifically, may help the virus evade immune responses. But more studies and clinical data are necessary to understand the full effect of the new addition.

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The Coronavirus Is Mutating, and That’s Fine (So Far)

SARS-CoV-2 has been slowly changing in small ways, without getting more dangerous.

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Washington’s COVID-19 outbreak may have begun a month later than we thought

People in protective gear load a stretcher-bound patient into an ambulance.

Enlarge / KIRKLAND, Wash.: A patient is shielded as they are put into an ambulance outside the Life Care Center of Kirkland on March 7, 2020. Several residents have died from COVID-19, and others have tested positive for the novel coronavirus. (credit: Getty | Karen Ducey)

When cases of COVID-19 began popping up in Washington state in late February, researchers were quick to dive into the genetics of the viruses infecting residents. Based on what they knew at the time, they hypothesized that those cases in late February were genetically linked to the very first case found in the state—one in a person who arrived in Washington on January 15 after traveling from Wuhan, China, where the outbreak began. The case was also the first infection identified in the whole of the United States.

If correct, the genetic hypothesis linking the late February cases to that very first case meant that early efforts to contain the pandemic coronavirus—isolating the initial patient, tracing contacts, etc.—had failed spectacularly. It also meant that the virus, SARS-CoV-2, had been cryptically circulating in the state for six weeks. And that would mean that, in addition to those early cases, there were potentially hundreds or thousands of others out there, undetected and possibly spreading the infection further.

The hypothesis played into state officials’ decision to issue some of the country’s earliest social-distancing measures. But now that we know far more about the genetics of circulating SARS-CoV-2 viruses, that hypothesis appears to be wrong.

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